Abstract:
:The patterns of expression of the Bcl-2, Bax, and Bcl-xL proteins were examined immunocytochemically in rat hippocampus and neocortex after severe hypobaric hypoxia (180 Torr for 3 h) and severe hypoxia preconditioned by intermittent mild hypoxia (360 Torr for 2 h daily, for 3 consecutive days, 24 h prior to severe hypoxia). As revealed by TUNEL assay, severe hypobaric hypoxia produced extensive apoptotic damage to the neurons of hippocampal CA1-CA4 and the neocortex but not the dentate gyrus granule cells. Remarkable posthypoxic up-regulation of Bax expression maximal at 24 h was detected in the CA1-CA4 areas of hippocampus and neocortex 3-72 h after severe hypoxia. The preconditioning to severe hypoxia protected neurons from the posthypoxic apoptotic transformations, the up-regulation of Bax expression, and resulted in persistent overexpression of Bcl-2 and Bcl-xL. We conclude that the protective action of hypoxic preconditioning is at least in part mediated by shifting of neuronal Bax/Bcl-2-Bcl-xL ratio to a favor of antiapoptotic proteins Bcl-2 and Bcl-xL.
journal_name
Brain Resjournal_title
Brain researchauthors
Rybnikova E,Sitnik N,Gluschenko T,Tjulkova E,Samoilov MOdoi
10.1016/j.brainres.2006.03.053subject
Has Abstractpub_date
2006-05-17 00:00:00pages
195-202issue
1eissn
0006-8993issn
1872-6240pii
S0006-8993(06)00805-5journal_volume
1089pub_type
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